Ocular inflammation is often associated with infiltration of either neutrophils or eosinophils. The current proposal will utilize a murine model for river blindness (onchocerciasis) in which both cell types are recruited to the cornea in a temporal manner after intrastromal injection of parasite antigens, i.e., an early neutrophilic infiltrate is replaced by eosinophils. As the presence of each cell type in the cornea reflects a balance between cell recruitment and survival within the tissue, specific aims of this proposal will determine the molecular events which regulate infiltration of neutrophils to the cornea. Specifically temporal expression of vascular adhesion molecules will be examined, as well as expression of cytokines and chemokines involved in neutrophil recruitment. The role of programmed cell death (apoptosis) in persistence of these cells will also be investigated. Results obtained from the proposed experiments are expected to be more broadly applicable to neutrophil-mediated ocular inflammation, and may identify possible targets for immune-based therapy.